Редактирование: MAB21L2

Protein mab-21-like 2

==Publications==

{{medline-entry
|title=The transcriptional profile of mesenchymal stem cell populations in primary osteoporosis is distinct and shows overexpression of osteogenic inhibitors.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/23028809
|abstract=Primary osteoporosis is an age-related disease characterized by an imbalance in bone homeostasis. While the resorptive aspect of the disease has been studied intensely, less is known about the anabolic part of the syndrome or presumptive deficiencies in bone regeneration. Multipotent mesenchymal stem cells ([[MSC]]) are the primary source of osteogenic regeneration. In the present study we aimed to unravel whether [[MSC]] biology is directly involved in the pathophysiology of the disease and therefore performed microarray analyses of h[[MSC]] of elderly patients (79-94 years old) suffering from osteoporosis (h[[MSC]]-OP). In comparison to age-matched controls we detected profound changes in the transcriptome in h[[MSC]]-OP, e.g. enhanced mRNA expression of known osteoporosis-associated genes (LRP5, [[RUNX2]], COL1A1) and of genes involved in osteoclastogenesis (CSF1, PTH1R), but most notably of genes coding for inhibitors of WNT and BMP signaling, such as Sclerostin and [[MAB21L2]]. These candidate genes indicate intrinsic deficiencies in self-renewal and differentiation potential in osteoporotic stem cells. We also compared both h[[MSC]]-OP and non-osteoporotic h[[MSC]]-old of elderly donors to h[[MSC]] of ∼30 years younger donors and found that the transcriptional changes acquired between the sixth and the ninth decade of life differed widely between osteoporotic and non-osteoporotic stem cells. In addition, we compared the osteoporotic transcriptome to long term-cultivated, senescent h[[MSC]] and detected some signs for pre-senescence in h[[MSC]]-OP.Our results suggest that in primary osteoporosis the transcriptomes of h[[MSC]] populations show distinct signatures and little overlap with non-osteoporotic aging, although we detected some hints for senescence-associated changes. While there are remarkable inter-individual variations as expected for polygenetic diseases, we could identify many susceptibility genes for osteoporosis known from genetic studies. We also found new candidates, e.g. [[MAB21L2]], a novel repressor of BMP-induced transcription. Such transcriptional changes may reflect epigenetic changes, which are part of a specific osteoporosis-associated aging process.
|mesh-terms=* Aged
* Aged, 80 and over
* Aging
* Bone Density
* Cellular Senescence
* Cluster Analysis
* Female
* Gene Expression Profiling
* Gene Expression Regulation
* Genetic Predisposition to Disease
* Humans
* Male
* Mesenchymal Stem Cells
* Middle Aged
* Oligonucleotide Array Sequence Analysis
* Osteogenesis
* Osteoporosis
* Osteoporotic Fractures
* Risk Factors

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3454401
}}